Chronic wounds can be caused by a variety of events, including surgery, prolonged bed rest, and traumatic injuries. Partial thickness wounds can include second degree burns, abrasions, and skin graft donor sites. Healing of these wounds can be problematic, especially in cases of diabetes mellitus or chronic immune disorders. Full thickness wounds have no skin remaining, and can be the result of trauma, diabetes (e.g., leg ulcers), and venous stasis disease, which can cause full thickness ulcers of the lower extremities. Full thickness wounds tend to heal very slowly. Proper wound care technique, including the use of wound dressings, is extremely important to successful chronic wound management. Chronic wounds affect an estimated four million people a year, resulting in health care costs in the billions of dollars.
The wound healing process involves a complex series of biological interactions at the cellular level, which can be grouped into three phases: hemostasis and inflammation, granulation tissue formation and reepithelization, and remodeling. Keratinocytes (epidermal cells that manufacture and contain keratin) migrate from wound edges to cover the wound. Growth factors such as transforming growth factor-β (TGF-β) play a critical role in stimulating the migration process. The migration occurs optimally under the cover of a moist layer.
Keratin proteins are present in a wide range of biological tissue, performing a structural role in skin, hair and other materials. Keratins extracted from hair have been shown to be a valuable component in wound dressings. Specifically, keratins have been found to be necessary for the reepithelization phase of the wound healing process.
Many wound dressings previously described require that the wound dressing be removed from the open wound after a certain time to be replaced by a new wound dressing because the wound dressing is no longer aiding the healing process, but remains on the wound. In wound dressings such as these, the wound dressing may become attached to the wound due to ingrowth of tissue into the wound dressing, and therefore removal of the wound dressing will re-traumatize the wound and inhibit the healing process.
Other previously described wound dressings comprising keratin have also failed to adequately treat chronic wounds because of an inability to maintain keratin in the wound for a period of time that allows the keratin to promote wound healing. Previously known wound dressings have attempted to use untreated soluble keratin as a component of the wound dressing. However, the untreated soluble keratin is absorbed too quickly and does not stay in the wound long enough to be used in the healing process, and therefore is ineffective in promoting wound healing.
Alternatively, previously described wound dressings comprising insoluble keratin have also failed to adequately treat chronic wounds. Insoluble keratins in wound dressing are not metabolized by the wound and therefore need to be removed from the wound. Removal of the insoluble keratin runs the risk of re-traumatizing the wound as discussed previously and therefore slows or sets-back the healing process. Furthermore, insoluble keratins do not posses the appropriate three-dimensional structure necessary to support maximum cell growth and proliferation. Thus, wound dressings comprising insoluble keratin protein fall short of adequately promoting wound healing.
Previously described wound dressings comprising keratin have also failed to adequately protect against oxidative stress in a wound environment. Sulfhydryl groups are vital in maintaining the oxidant-antioxidant balance within a cell and preventing situations of oxidative stress. However, no previously described wound dressings comprising keratin promote species such as glutathione to combat oxidative stress.